microRNA-29a functions as a tumor suppressor in nasopharyngeal carcinoma 5-8F cells through targeting VEGF
محل انتشار: مجله علوم پایه پزشکی ایران، دوره: 22، شماره: 5
سال انتشار: 1398
نوع سند: مقاله ژورنالی
زبان: انگلیسی
مشاهده: 298
فایل این مقاله در 6 صفحه با فرمت PDF قابل دریافت می باشد
- صدور گواهی نمایه سازی
- من نویسنده این مقاله هستم
استخراج به نرم افزارهای پژوهشی:
شناسه ملی سند علمی:
JR_IJBMS-22-5_012
تاریخ نمایه سازی: 20 مهر 1398
چکیده مقاله:
Objective(s): microRNA-29 (miR-29) family miRNAs have been mentioned as tumor suppressive genes in several human cancers. The purpose of this study was to investigate the function of miR-29a in nasopharyngeal carcinoma (NPC) cells. Materials and Methods: Human NPC cell line 5-8F was transfected with mimic, inhibitor or scrambled controls specific for miR-29a. Subsequently, cell viability, migration, apoptosis and expression changes of VEGF were assessed by trypan blue staining, MTT assay, transwell assay, flow cytometry, Western blot and RT-qPCR. TargetScan online database was used to predict the targets of miR-29a, and luciferase reporter assay was carried out for testing the targeting relationship between VEGF and miR-29a. Western blot analysis was performed to determine the expression changes of core proteins in PI3K/AKT and JAK/STAT pathways. Results: Overexpression of miR-29a suppressed 5-8F cells viability and relative migration, but increased apoptotic cell rate. Consistently, Bcl-2 was downregulated, Bax was upregulated, and caspase-3 and -9 were cleaved by miR-29a overexpression. VEGF was a target gene of miR-29a. Besides, VEGF silence exerted similar effects like miR-29a, as the viability and migration were repressed and apoptosis was induced. Finally, we found that PI3K/AKT and JAK/STAT pathways were deactivated by miR-29a or VEGF silence. Conclusion: These findings highlighted the tumor suppressive effects of miR-29a on NPC cells, as its overexpression inhibited 5-8F cells viability, migration, and induced apoptosis. miR-29a exerted tumor suppressive functions might be via targeting VEGF and deactivating PI3K/AKT and JAK/STAT pathways.
کلیدواژه ها:
نویسندگان
Qingyuan Shi
Department of Otorhinolaryngology, HwaMei Hospital, University of Chinese Academy of Sciences (Ningbo No.۲ Hospital), Ningbo, Zhejiang ۳۱۵۰۱۰, P.R.China
Jinhua Dai
Department of Clinical Laboratory, HwaMei Hospital, University of Chinese Academy of Sciences (Ningbo No.۲ Hospital), Ningbo, Zhejiang ۳۱۵۰۱۰, P.R.China
Lizhen Huang
Department of Otorhinolaryngology, HwaMei Hospital, University of Chinese Academy of Sciences (Ningbo No.۲ Hospital), Ningbo, Zhejiang ۳۱۵۰۱۰, P.R.China
مراجع و منابع این مقاله:
لیست زیر مراجع و منابع استفاده شده در این مقاله را نمایش می دهد. این مراجع به صورت کاملا ماشینی و بر اساس هوش مصنوعی استخراج شده اند و لذا ممکن است دارای اشکالاتی باشند که به مرور زمان دقت استخراج این محتوا افزایش می یابد. مراجعی که مقالات مربوط به آنها در سیویلیکا نمایه شده و پیدا شده اند، به خود مقاله لینک شده اند :